A novel experimental approach will be employed to examine the reflex control of left ventricular contractility by the aortic body chemoreceptors. Aortic bodies of anesthetized, open chest dogs will be stimulated physiologically 1) by reducing oxygen tension, 2) by raising carbon dioxide tension, or 3) by altering independently pH of blood perfusing the aortic arch and pharmacologically by nicotine. To prevent other mechanisms from changing myocardial function during aortic body activation: 1) The brachiocephalic and left common coronary arteries will be perfused independently at controlled pressure with oxygenated blood obtained from a support dog; venous blood from these regions will be returned to the support dog. 2) Depth and rate of ventilation will be fixed. 3) Mean aortic pressure will be held constant. 4) Left ventricular end-diastolic pressure will be regulated. 5) Heart rate will be set with a pacing electrode. Myocardial contractility will be assessed by: 1) left ventricular dP/dt max, 2) Walton-Brodie strain-gauges, 3) ventricular function curves. Myocardial contractility and myocardial oxygen consumption will be correlated during stimulation of aortic bodies. Transmural distribution of left ventricular blood flow will be evaluated with radioactive microspheres, so that changes in strain-gauge output and blood flow can be correlated on a regional basis. Myocardial contractility will be measured during independent, stepwise variations in oxygen tension, carbon dioxide tension, and pH, so that 1) stimulus thresholds can be defined and 2) stimulus-response curves can be generated. The level of these constituents will also be varied stimultaneously to assess their interaction in stimulating the aortic bodies. Autonomic blocking drugs will be used to characterize the efferent limb of the aortic body-cardiac reflex. Interactions between the aortic body reflex and other cardiovascular reflexes in neural regulation of cardiac function will be examined. This study will define for the first time the contribution of the aortic bodies to changes in cardiac function during disturbances in arterial blood gases, such as occur clinically with pulmonary disease or cardiac failure.